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Veterinary Virology > Order: Herpesvirales > Flashcards

Order: Herpesvirales Flashcards

1
Q

Where does Herpesvirus get its name?

A

Herpes = (Greek) herpein = to creep

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2
Q

What are the 3 subfamilies of Herpesviridae?

A
  1. ALPHA: huma herpesvirus 1,3; gallid herpesvirus 1, 2; chelonid herpesvirus 5; pseudorabies - restricted to a single host, with a rapid lytic cycle
  2. BETA: cytomegalovirus, muromegalovirus, proboscivirus, roseolovirus - highly restricted host range, with slow replicative cycle and delayed cell lysis
  3. GAMMA: lymphocryptovirus, macavirus, percavirus, rhadinovirus - narrow host range, with latency in lymphocytes
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3
Q

What is the difference between Alloherpesvirus and Malacoherpesvirus?

A
  • fish and reptiles: Ictalurivirus, Salmonivirus, Cyprinivirus, Batrachovirus
  • oysters and edible mollusks: Ostreavirus, Aurivirus
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4
Q

What is the morphology of the virion, tegument, envelope, capsid, and core of Herpesviruses?

A

VIRION: size varies from 130-300 nm due to thickness of tegument
TEGUMENT: protein structure between capsid and envelop
ENVELOPE: trilaminar membrane derived from cellular membrane, containing glycoprotein spikes
CAPSID: spherical icosahedral, 162 capsomeres
CORE: linear dsDNA

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5
Q

Where do Herpesviruses replicate?

A

within the nucleus (budding)

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6
Q

What are 5 important features of Herpesviruses?

A
  1. genome encodes for many enzymes involved in nucleic acid metabolism and protein processing
  2. establish latent infections
  3. lifelong persistence
  4. significant cause of death in immunocompromised hosts
  5. can cause cancer
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7
Q

What is present at the terminal ends of the Herpesvirus genome? What 2 unique regions are also present? What are they bound by?

A

repeated sequences (also present internally)

  1. unique long (UL)
  2. unique short (US)
    - inverted repeats (ITR)
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8
Q

How does the production of Herpesvirus progeny affect the host cell?

A

host cell distortion

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9
Q

What is infection with Herpesvirus like?

A

persistent infection with periodic/continuous shedding
- can remain latent in host cells

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10
Q

Where do the 3 subfamilies of Herpesvirales infect? Which ones tend to be clinically silent in mammals?

A

ALPHA: neurons
BETA: monocytes
GAMMA: lymphocytes

beta and gamma

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11
Q

Severe Herpesvirus infections are most common at what age? What kind of infection is established?

A

very young animals

systemic infection —> cell-associated viremia detectable during primary infection

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12
Q

Herpesvirus replication cycle:

A
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13
Q

When does Herpesvirus capsids form? What is characteristic of Herpesvirus inclusion bodies?

A

when it buds through the host’s nuclear envelop

intranuclear “owl eye” inclusion bodies

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14
Q

How is Herpesvius able to undergo latent replication?

A

replication of circular episome in tandem with host cell DNA using host’s replication machinery

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15
Q

What are the major 4 reasons that Herpesviruses are difficult to control?

A
  1. infect crucial tissues: brain, maternal placenta
  2. all become latent (as circular DNA in the nuclei of ganglia of lymphocytes) in recovered animals
  3. subsequent reactivation during stress causes disease or tumors
  4. all are cell-associated and can spread between cells by cell fusion
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16
Q

What are the 2 possible outcomes of Herpesvirus infection?

A
  1. LYTIC: destruction of infected cells due to alteration in biochemical and biological processes
  2. NON-LYTIC: integrate within host cell genome resulting in distortion or change in cell nucleus, chane in appearance of cell membrane, or appearance of viral protein (gD) in cell membrane
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17
Q

What are the 9 clinical manifestations of Herpes simplex virus? What is their host?

A

(humans)
1. acute gingivostomatitis
2. herpes labialis (cold sores)
3. ocular herpes
4. herpes genitalis
5. cutaneous herpes
6. meningitis
7. encephalitis
8. neonatal herpes
9. keratoconjunctivitis (corneal ulcers)

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18
Q

In what 3 ways is Herpes simplex virus infection diagnosed?

A
  1. CPE —> ballooning
  2. positive immunofluorescence tests of epithelial cells
  3. stained smears of materials from HSV lesion
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19
Q

What are the 2 groups of Equine Herpesvirus?

A
  1. ALPHA: EHV-1, 3, 4, 9
  2. BETA: EHV-2, 5
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20
Q

What are the clinical manifestations of Equine Herpesvirus-1, 2, 3, 4, 5, 8, and 9?

A

EHV-1 = equine abortion virus, with respiratory effects and encephalomyelitis (neurological, respiratory, abortion, natal death)
EHV-2 = granulomatous dermatitis
EHV-3 = genital lesions (Equine Coital Exanthema Virus) affecting external genitalia (no effect on fertility)
EHV-4 = Equine Rhinopneumonitis syndrome; nonfatal upper respiratory disease in foals
EHV-5 = equine multinodular pulmonary fibrosis (EMNPF)
EVH-8 = rhinitis
EVH-9 = asymptomatic; severe disease in other species

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21
Q

How is Equine Herpesvirus usually transmitted? How else can it be transmitted?

A

venereal
- direct or indirect contact with infectious nasal secretions, aborted fetuses, placentas, or placental fluids

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22
Q

How do the pathogenic mechanisms of EHV-1 and EHV-4 differ?

A

EHV-1 = predilection for vascular endothelium, especially nasal mucosa, lungs, adrenal glands, thyroid, and CNS and is able to access peripheral tissues via cell-associate viremia (abortion, neurologic disease)

EHV-4 = infection restricted to respiratory tract epithelium and associated LNs

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23
Q

What is the most common clinical sign that precedes other signs of EHV infection?

A

fever

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24
Q

What respiratory disease can EHV cause?

A
  • fever, coughing, nasal discharge
  • influenza
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25
Q

When do abortions typically occur during pregnancy when infected with EHV?

A

late in pregnancy (> 8 months)

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26
Q

Which EHV is associated with neurological signs? How can symptoms range?

A

EHV-1

mild incoordination —> severe posterior paralysis

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27
Q

Does EHV infection affect urination and defecation?

A

yes - inability to pass urine or manure

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28
Q

How can EHV lead to neuronal necrosis?

A

vasculitis —> thrombosis —> ischemic condition in spinal cord —> neuronal anoxia —> neuronal necrosis

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29
Q

What is the pathogenesis of EHV-1?

A
  • infects epithelial cells of respiratory tract
  • replicates and sheds
  • dissemination through respiratory tract
  • reaches LNs
  • virus is circulated by leukocytes
  • dissemination to distant targets of DNA and reproductive tract
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30
Q

How is EHV-1 transmitted to the fetus?

A

spreads by cell-to-cell contact to the fetus through capillary endothelium in the umbilical cord, allowing infection of endometrial cells, causing uterine pathology, premature placental separation, and fetus anoxia
- virus-negative fetus

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31
Q

EHV-1 pathogenesis - abortion:

A
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32
Q

What are the complications of EHV-1 infections in pregnant mares, full-term foals, and infected fetuses?

A

MARES: asymptomatic with abortion 4-5 months later

FULL-TERM FOALS: general weakness, pneumonia, death

INFECTED FETUSES: abortion in late pregnancy results in fresh death due to suffocation, following rapid placental separation

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33
Q

ENH-4 can cause abortion. How does this compare to EHV-1?

A

EHV-4 may cause isolated abortions, but it doesn’t cause abortion storms

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34
Q

General pathogenesis of EHV-1 and EHV-4:

A
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35
Q

What 4 EHV have the ability to cause equine viral rhinopneumonitis?

A

EHV-1, 2, 3, 4

1 = extends beyond respiratory tract via viremia
4 = restricted to URT

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36
Q

What lesion is associated with EHV-2?

A

granulomatous dermatitis —> multifocal to coalescing areas of necrosis marked by histiocytic cell infiltration and the presence of giant cells

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37
Q

What is characteristic of EHV-3 infection?

A

(Equine Coital Exanthema)
- acute sexually transmitted disease causing papules, vesicles, pustules, and ulcers on the penis and prepuce of stallions and the external genitalia and peripheral skin of mares

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38
Q

How is the genitalia commonly affected by EHV-3?

A

lesions heal within 14 days, leaving depigmented patches on the vulva, penis, and prepuce —> typically remains for life, which helps identify previously infection individuals (carriers)

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39
Q

How is EHV infection diagnosed?

A
  • case history
  • clinical signs
  • virus isolation from aborted fetus
  • PCR
  • serology: serum neutralization test, complement fixation test
  • hematology: leukopenia
40
Q

How is EHV infection controlled?

A

vaccination at an early age with periodic boosters depending on management
(can reduce incidence and severity)

41
Q

What causes Pseudorabies?

A

Alphaherpesvirus, Porcine herpesvirus-1
- Genus: Varicellovirus

(Aujesky’s Disease, Mad Itch)

42
Q

What is the natural host of Pseudorabies? Dead-end hosts?

A
  • pigs (unaffected)
  • dogs, cats, cattle, etc. (fatal)
43
Q

How does morbidity of Pseudorabies compare in piglets and adults? How is mortality affected by age? When is Pseudorabies always fatal?

A

PIGLETS: up to 100% morbidity
ADULTS: no signs (20% abortions)

mortality is highest in younger animals and decreases with age

in all species other than pigs

44
Q

What are the 3 most common modes of transmission of Pseudorabies? 2 additional?

A
  • respiratory
  • oral
  • nose-to-nose contact
  • aerosol
  • fomites (contaminated bedding, water, meat products, carcasses)
45
Q

What are common clinical signs of Pseudorabies in <1 week old piglets? Older/weaned piglets? Adult pigs?

A
  • fever, listlessness, anorexia
  • neurological signs: tremors, paddling, seizures, dog-sitting
  • high mortality within 24-36 hours
  • respiratory, neurological, vomiting
  • lower mortality
  • mild/subclinical
  • respiratory and neurologic signs
  • reproductive signs in pregnant sows
46
Q

What is the pathogenesis of Pseudorabies in pigs?

A
  • replicates in tonsils and oral pharyngeal epithelium, which causes mild respiratory signs
  • follows trigeminal nerve to ganglia to indue latent infection and CNS signs
  • can cross placenta
47
Q

What is the pathogenesis of Pseudorabies in dead-end hosts based on entry?

A
  • enter via oral routes/ingestion
  • virus follows autonomic nerves to spinal cord and brain, causing CNS signs, rapid breathing, pruritus
  • enter via bite wounds
  • follows nerves to spinal cord and CNS
  • intense pruritus (mad itch) with self mutilation at bite site
  • death
48
Q

What are the most common clinical signs of Pseudorabies in cattle/sheep and dogs/cats?

A

CATTLE/SHEEP: intense pruritus with licking, rubbing, gnawing, and self-mutilation; neurological signs

DOGS/CATS: resembles rabies, sudden death in 1-2 days

49
Q

What are the 3 characteristic necropsy findings in Pseudorabies? What is especially common in pigs and other species?

A
  1. liver necrosis
  2. neutrophil infiltration
  3. tonsil necrosis

PIGS: neurological - nonsuppurative meningoencephalitis; respiratory - necrolytic tonsilitis, bronchitis, bronchiolitis, and alveolitis; focal necrosis

OTHERS: spinal cord lesions

50
Q

What 4 vaccines are available for Pseudorabies?

A
  1. inactivated
  2. modified live
  3. deletion mutant
  4. sub-unit + immune-stimulating complex (ISCOMs)
51
Q

What are 5 ways that Pseudorabies is controlled?

A
  1. IMMEDIATELY notify authorities
    2, quarantine isolation and testing of new animals
  2. test and slaughter (UK)
  3. biosecurity - prevent entry, double fencing
  4. disinfection - phenols, quaternary ammonium compounds, heat, sunlight
52
Q

What are the main 4 classes of Bovine Herpesvirus?

A

BHV-1.1 = respiratory disease, abortion
BHV-1.2a = infectious balanoposthitis/infectious pustular vulvovaginitis syndrome, abortion
BHV-1.2b = infectious balanoposthitis/infectious pustular vulvovaginitis syndrome, NO abortion
BHV-2 = Bovine Ulcerative Mamillitis (Allerton virus)

53
Q

In what 4 ways does BHV-1 present?

A
  1. ocular
  2. genital - abortion, vulvovaginitis, infectious balanoposthitis
  3. respiratory - infectious bovine rhinotracheitis (fatal bronchopneumonia)
  4. neurologic - meningoencephalitis in young calves
54
Q

What is the pathogenesis BHV-1?

A
  • virus replicates in the URT
  • spreads via lacrimal ducts

(genital infections are most likely venereally transmitted)

55
Q

What 4 actions make BHV-1 able to cause infection?

A
  1. induces pro-inflammatory cytokine production
  2. downregulates MHC-I
  3. causes apoptosis of CD4 lymphocytes
  4. causes transient immuosuppression
56
Q

What 2 nasal lesions are characteristic of BHV-1 infection?

A
  1. red-tinged serous fluids from eroded vesicles (red nose)
  2. vesicle and/or eroded vesicles within nostril
57
Q

What are the characteristic mucosal lesions in BHV-1 infection?

A

adherent, whitish, necrotic material raised above the mucosal surface

58
Q

When do most abortions caused by BHV-1 occur? What 2 neurological signs are common?

A

within the last 4 months of gestation (earlier abortions are not generally detected)

  1. incoordination
  2. opisthotonus
59
Q

What 5 brain lesions are common in BHV-1 infection?

A
  1. hyperemia of leptomeninges
  2. swollen rostral telencephalon
  3. malacia of cortex
  4. neuronal necrosis
  5. mononuclear perivascular cuffing
60
Q

How is BHV-1 infection diagnosed?

A
  • case history, clinical signs, PM lesions
  • proper sampling (feces, fecal swab, nasal swab)
  • detection of viral particles by EM
  • viral isolation from conjunctival swabs and placenta
  • indirect fluorescent antibody assay, immunoperoxidase
  • PCR
  • serology: virus neutralization, ELISA
61
Q

How is BHV-1 infection controlled?

A
  • modified live vaccine (intranasal, IM)
  • inactivated (IM)
62
Q

What disease does BHV-2 cause?

A

Pseudolumpy skin disease; bovine viral mammillitis; Allerton virus

63
Q

In what 3 ways does BHV-2 infection present? How is it typically transmitted?

A
  1. generalized skin disease
  2. mammilitis
  3. stomatitis

biting flies

64
Q

What 3 things is BHV-2 infection diagnosis based on?

A
  1. clincal signs
  2. viral isolation in tissue culture
  3. serology in paired samples demonstrating increase in antibodies
65
Q

What is Malignant Catarrhal Fever?

A

clinically dramatic and often lethal infection of many species of Bovidae and Cervidae caused by MCFV (Macavirus, Gammaherpesvirinae)

  • notifiable disease to OIE
66
Q

What are 8 common clinical signs of Malignant Catarrhal Fever?

A
  1. acute, high fever
  2. catarrhal inflammation
  3. corneal edema and opacity (blue eye)
  4. enlarged lymph nodes
  5. skin lesions
  6. diarhea
  7. severe inflammatory lesions of muzzle, eye, respiratory and digestive tract
67
Q

What are common carriers of Malignant Catarrhal Fever? What species are clinically susceptible hosts?

A
  • sheep
  • deer
  • cows
  • bison
68
Q

What are the 2 main Caprine Herpesviruses?

A

CpHV-1 = young goats with enteric signs and necrosis/ulceration in the rumen, cecum, and colon; can also cause abortion, vulvovaginitis, and balanoposthitis

CpHV-2 = captive sika deer with nasal discharge, oral vesicles on muzzle and tongue, and growth lesions on kidney and lung

69
Q

In what 4 ways does Canid Herpesvirus-1 infection typically present?

A
  1. neonatal deaths, abortion, and mummification
  2. fatal systemic infection in newborn puppies
  3. genital lesions
  4. healthy dog with an infertility history
70
Q

What complex is Canid Herpesvirus-1 typically part of? Are vaccines available? What therapy is typically used?

A
  • canine respiratory disease complex (kennel cough)
  • no
  • Acyclovir
71
Q

What does Felid Herpesvirus-1 cause? How does this typically present? What 5 conditions are typically associated?

A

feline viral rhinotracheitis and upper respiratory disease

hunched-up appearance with head on the floor and a prominent third eyelid

  1. conjunctivitis
  2. ulcerative keratitis
  3. ulcerative stomatitis
  4. abortions
  5. pneumonia + dyspnea
72
Q

How does Feline Herpesvirus-1 typically spread?

A

cat-to-cat by direct contact through infectious discharges from nose, eyes, and throat, and aerosolized microdroplets

73
Q

What is characteristic of Feline Herpesvirus-1 reactivation?

A

dendritic ulcers in the cornea with possible perforation

74
Q

What is Marek’s Disease? What are the 3 serotypes?

A

lymphoproliferative, neuropathic, and highly contagious disease of chickens (+ pheasants, quails, turkeys)

SEROTYPE 1: pathogenic and oncogenic (mildly virulent, virulent, highly virulent)
SEROTYPE 2: avirulent and non-oncogenic
SEROTYPE 3: avirulent, turkeys only (vaccine strains)

75
Q

What are 3 common signs of Marek’s disease? What is most common in broilers?

A
  1. mononuclear (lymphoblast) infiltration in peripheral nerves and other organs
  2. lymphomas in gonads, heart, lungs, bursa, skin, muscles
  3. ataxy, paralysis, macroscopic thickening of peripheral nerves

neoplastic changes

76
Q

What are the main 4 groupings of Marek’s disease based on clinical presentations?

A
  1. CLASSICAL: neurolymphomatosis, loss of coordination, asymmetric paresis/paralysis
  2. ACUTE: expansive burst in flock, depression, ataxy, paralysis, significant mortality without neurological changes
  3. EYE: lymphoblastoid infiltration of pupil, blindness
  4. SKIN: round, nodular lesions in feather follicles
77
Q

How is Marek’s Disease virus typically transmitted? In what way is it not transmitted? How does it survive in the environment?

A
  • highly contageous, concentrates in feather follicles and spreads with bird-to-bird contact or contact with infected dust/dander
  • through the egg, chicks will not be able to be born with it
  • can survive for months in chicken-house dust and litter
78
Q

What is the most common form of Marek’s Disease? What other form in observed?

A
  • NEURAL FORM (classical): affecting sciatic nerve
  • VISCERAL FORM: enlargement of peripheral nerves, leg paresis with one leg extended forward and the other backward, starvation, death
79
Q

Signs of the visceral form of Marek’s disease is less specific. What are some examples?

A
  • depression, loss of appetite
  • anemia (pale combs)
  • dehydration
  • diarrhea
  • tumors on internal organs, including the bursa of Fabricius, ovaries, liver, and lungs
  • lymphomas on lung and heart
  • death without clinical signs
80
Q

How does cutaneous and ocular Marek’s disease present?

A

CUTANEOUS: proliferating lymphocytes deposited in skin, producing nodular lesions and ulcers in feather follicles

OCULAR: iris involvement, blindness

81
Q

What is the preferred vaccine for Marek’s disease?

A

Tuekry Herpesvirus vaccine —> high antigenic dose

82
Q

How does Marek’s Disease compare to Avian Leukosis?

A

MDV: Herpesvirus etiology, T lymphocytes are targeted, 4 weeks age of onset, paralysis, intranuclear inclusion bodies

ALV: Retrovirus etiology, hematopoietic cells targeted, 16 weeks age of onset, no paralysis or intranuclear inclusion bodies

83
Q

What 2 viruses cause dyspnea in pullets (young hens)?

A
  1. infectious laryngotracheitis virus
  2. gallidherpesvirus-1
84
Q

Why does gallidherpesvirus-1 cause dyspnea, coughing, and rales?

A

causes the production of a diphtheritic membrane that may form a tube the length of the trachea and occlude air flow

85
Q

What are the 2 possible hosts of gallidherpesvirus-1? How is it transmitted in a flock?

A
  1. chickens
  2. pheasants
  • introduced by a carrier and mostly transmitted by inhalation (+ ingestion)
86
Q

What is the pathogenesis of Gallidherpesvirus-1?

A

severe laryngotracheitis characterized by necrosis, hemorrhage, and the formation of diphtheritic membranes. causing death by asphyxiation

87
Q

What are 5 clinical features of infectious laryngotracheitis caused by gallidherpesvirus-1?

A
  1. most common in chicken 4-18 months
  2. marked respiratory disease: extension and slinging of neck during inspiration
  3. head pressing, resting on breast during exhalation, coughing, rattling
  4. cough up bloody mucus that stains walls and posts
  5. morbidity = 100%, mortality = 20-70% depending on the virulence of the strain
88
Q

What causes duck viral enteritis? What are 9 symptoms?

A

Anatid (alpha)Herpesvirus-1

  1. anorexia, watery diarrhea
  2. listlessness, ataxia leading to recumbency with outstretched wings and an extended neck
  3. nasal discharge
  4. ruffled, dull feathers
  5. adherent eyelids
  6. photophobia*
  7. extreme thirst
89
Q

What 5 postmortem lesions are commonly found with duck viral enteritis?

A
  1. multifocal ulceration in intestinal mucosa
  2. enlarged and mottled spleen
  3. mottled thymus with petechial hemorrhage
  4. inflammation and hemorrhage of proventriculus and gizzard
  5. hemorrhagic intestine with an annular band
  6. diffuse petechial hemorrhage in liver
90
Q

How is duck viral enteritis transmitted?

A

contact between susceptible captive waterfowl and wild, free-flying waterfowl

91
Q

What does Psittacid Herpesvirus-1 cause?

A

Pacheo’s Disease - acute, contagious, and lethal disease of macaws, Amazon parrots, monk, parakeets, and conures, causing hepatomegaly, splenomegaly, and petechial hemorrhage in the pericardium (+ splenic and liver necrosis with inclusion bodies)

92
Q

How do Old World parrots factor into Pacheo’s Disease? How is it transmitted? Is there a vaccine?

A

resistant to disease and can be a carrier

ingestion/inhalation of contaminated feces and oral/pharyngeal secretions

no

93
Q

What causes inclusion body disease in falcons? What 2 species are most commonly affected? What does this virus have a marked affinity for?

A

Falconid Herpesvirus-1

  1. American kestrels
  2. great horned owls

reticuloendothelial system and hepatocytes, producing focal to diffuse necrosis and intranuclear inclusion body formation

94
Q

How does Elephant Endotheliotropic Herpesvirus affect newborn and adult Asian elephants? What is the main lesion?

A

NEWBORN: 20% mortality
ASIAN ELEPHANT: vague signs, like lethargy and inappetence with death in 24 hrs

massive and generalized hemorrhages (diathesis) due to replication in the vascular endothelium

95
Q

What does Channel Catfish Virus Disease result in? What are 6 common signs?

A

presence of intranuclear inclusion bodies and extensive syncytium formation

  1. reduced feeding activity and high mortality in fry = first sign
  2. exophthalmos and hemorrhaging of fins and ventral abdomen
  3. swelling of abdominal cavity containing fluid
  4. dark and enlarged spleen
  5. pale and enlarged kidney
  6. large numbers of fish aggregating around the edges of hatching troughs or pools, remaining motionless in a head-up, tail-down position
96
Q

How is the family Alloherpesviridae distinct from other herpesviruses? What are the main 2 divisions?

A

distinct genome sequences and high level of host specificity, modulation of host defenses, long-term latency, and epithelotropic tendencies

  1. Cyprinid herpesvirus-3 (Koi)
  2. Salmonid herpesvirus-1 (low mortality), 2 (oncogenic, pathogenic in young), 3 (high mortality)

Veterinary Virology (25 decks)

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